Why is it called “Hashimoto’s” Hashimoto’s disease is an alias for chronic lymphocytic thyroiditis, which was first discovered by a Japanese man named Hashimoto, so the medical community named it after him. Hashimoto of Kyushu University in Japan first (1912) reported four cases in the German Medical Journal, so it was named Hashimoto (Hashimoto) thyroiditis (HT), the most common thyroid inflammation in the clinic. The incidence has increased rapidly in recent years and has been reported to be similar to the incidence of hyperthyroidism. It is the most common cause of goitre and acquired hypothyroidism in children and adolescents. Unrelenting fatigue and goiter are the relatively prominent clinical manifestations. It is usually painless, slow to develop, and may also have light pressure pain; nodules may be present on the surface. In middle-aged women with diffuse goiter, especially when accompanied by conus lobe enlargement, the disease should be suspected, regardless of thyroid function. Patients with Hashimoto’s thyroiditis can have hyperthyroidism, normal thyroid function, or can present with hypofunction. The first consideration is Hashimoto’s thyroiditis when there is no drug factor for the change from hyperthyroidism to hypothyroidism. Serum thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) levels are among the gold indicators for detecting Hashimoto’s thyroiditis, especially in those with increased serum TSH levels. However, some patients require multiple tests to detect increased antibody titers, while others have consistently low titers of anti-thyroid antibodies. Therefore, fine needle aspiration or surgical biopsy for pathology should be considered when necessary. How to deal with Hashimoto Normally, the normal tissues and organs of the body are protected by the immune function and are not destroyed by the immune function. In patients with chronic lymphatic thyroiditis, immune dysfunction produces substances that can destroy thyroid tissue. These substances include thyroid autoantibodies such as thyroglobulin antibodies and thyroid peroxidase antibodies. Higher antibodies suggest that the autoimmunity may be more intense and that the thyroid gland is in a destructive stage. If thyroid function is normal, follow-up is the main measure in the management of Hashimoto’s thyroiditis. Follow-up visits every 3 months to 6 months are generally recommended, mainly to check thyroid function and, if necessary, to perform thyroid ultrasonography; in cases of hypothyroidism or apparent subclinical hypothyroidism, thyroid hormone replacement therapy must be used. The goal of treatment is to restore serum TSH and thyroid hormone levels to the normal range. Adequate amounts of thyroid preparations are effective for suppressing TSH and receding goiter; in combined hyperthyroidism, propranolol is given in mild cases, and small doses of antithyroid drugs are given in moderate and severe cases; when Hashimoto’s thyroiditis causes rapid enlargement of the thyroid gland with symptoms of compression, pharmacological doses of glucocorticoids are effective. In this case, glucocorticosteroids can only be used for a short period of time, and the side effects of long-term use will outweigh the efficacy; Hashimoto’s disease combined with nodules requires attention to determine the nature of the nodules, and if the nodules are still small, regular ultrasound review is recommended, the first time at 3 months. If the patient has concerns, needle aspiration biopsy with cytology can be performed, and if the diagnosis is still unclear, surgical excision can be performed. The incidence of Hashimoto’s thyroiditis combined with thyroid cancer, especially papillary thyroid cancer, has been on the rise in recent years. Hashimoto’s thyroiditis may be one of the high-risk factors for the development of thyroid cancer. For women with known positive TPOAb before pregnancy, thyroid function must be checked to confirm normal thyroid function before pregnancy; thyroid function should be reviewed regularly during pregnancy, and L-T4 treatment should be given immediately in case of hypothyroidism or low T4emia, otherwise it will lead to insufficient supply of thyroid hormones to the fetus and affect its neurodevelopment. For women with pre-pregnancy TPOAb positivity with clinical hypothyroidism or subclinical hypothyroidism, thyroid function must be corrected to normal before pregnancy can occur. “Hashimoto’s antibodies are extremely persistent. There is no treatment for autoimmune thyroiditis that addresses the cause. Infection and iodide in the diet are two environmental factors in the development of the disease. Take care not to get infected and not to consume more iodide in general. Limiting iodine intake to a safe range (urinary iodine in the range of 100-200 μg/L) may help to slow down the progression of autoimmune destruction of the thyroid gland. It is important to emphasize that there are no effective drugs to bring down autoantibodies, and the rise and fall of autoantibodies can be regulated almost only by oneself. When I treat patients, I find that many of them have a common “problem”: the stubbornness of the thyroid-related antibodies (Tpoab, TGab, etc.) and the difficulty in decreasing their levels. In recent years, various new methods have emerged to treat this disease from the perspective of immunomodulation, which can lead to a decrease in the level of autoantibodies in the thyroid gland, a reduction in the size of the enlarged thyroid gland, and an improvement in the patient’s self-perceived symptoms. The use of immune agents to treat autoimmune thyroiditis often requires prolonged medication with side effects, and experience needs to be accumulated. It has been suggested that the trace element selenium can reduce or inhibit the immune damage of autoimmune thyroiditis. Selenium is an essential trace element in human body and an antioxidant. It has important physiological functions such as anti-aging, anti-tumor, cardiovascular protection, and antagonism to heavy metal toxicity. Selenium can improve the immune function of human body. In 2003, the U.S. Food and Drug Administration (FDA) confirmed that selenium is a cancer suppressant, and selenium supplementation can reduce the mortality rate of tumors by half, and high-dose selenium supplementation can reduce the toxicity of chemotherapy drug treatment and significantly improve the effect of radiotherapy and chemotherapy treatment. There is no need to fear “Hashimoto” Most autoimmune thyroiditis has a good long-term prognosis and is a benign process. The natural progression of the disease to hypothyroidism is very slow. It was previously thought that hypothyroidism caused by autoimmune thyroiditis was permanent. Recent data show that some patients with hypothyroidism caused by autoimmune thyroiditis can be temporarily hypothyroid and have spontaneous recovery of thyroid function in about 20% of cases when replaced with thyroid hormone.